It has been argued that viruses have sex. Bacteria definitely do; the process is called conjugation. The bacteria E. coli, found in your intestines, even grows a tiny penis. It is not known how they self-identify. Since they are neat and tidy, one can’t tell whether they have had sex or not. They were discovered in the act by Joshua Lederberg and Edward Tatum, who spent many pleasurable hours sneaking glimpses through the microscope, and drawing explicit pictures.
Viruses, more primitive and bestial than bacteria, go about it more like Frankenstein’s monster, occasionally grabbing pieces of the genomes of other viruses in the same infected cell. These special forms of mutation are much less common than the simple, single point substitution, addition or deletion.
Occurring at a predictable rate, simple mutations provide a means to estimate the evolutionary distance in time from an ancestral strain. This was used to debunk the idea that CDC sponsored research at the Wuhan Institute of Virology could have mutated into COVID-19; the viruses of the CDC sanctioned activity are too distant in time.
The miracle of life stems from the ability of both DNA and RNA to serve as templates for duplication of the genetic code, and synthesis of the substances cells and viruses are made of. A second miracle is the self-assembly of these substances into the structures of life. Multiple organic catalysts operate in concert with incredible precision.
The way a coronavirus accomplishes this is not straightforward. It routinely uses a method, copy-choice template switching, similar to the repair process for defective replication, which follows.
Sometimes a template breaks in use. Then, with devilish ingenuity that makes you wonder about the anthropic universe, repair enzymes attempt to find a replacement template and continue the transcription. Sometimes a proofreading enzyme detects a transcription error. Molecular shears snip out a segment, splicing in a new transcription.
How does the repair process have a hope of finding the correct alignment in a substitute template, a strand-like molecule thousands of atoms long? It does what you might do, holding a long ticker tape in your hands. You look for a sequence of symbols that look familiar. The repair enzymes do this too, matching some sequence of the new template with a location on the already duplicated strand, a homologous match. The match does not have to be at the break. Close is good enough.
The normal replication of a corona virus resembles this complex cascade. It can result in a more complex mutation. The inside of a cell is hot, full of bouncing, vibrating molecules, which jiggle and break from constant impact with other atoms. RNA templates are torn away from their partially constructed targets multiple times in the duplication process. A template may fly off and go missing.
Then the repair process searches for another template. There are many floating in the cytoplasm of an infected cell. If the cell is infected by a second species of virus related to the first, the repair may grab a template from the wrong virus, particularly if it finds a homologous match.
- (nference) Omicron variant of SARS-CoV-2 harbors a unique insertion mutation of putative viral or human genomic origin.
This is homologous recombination. Such an event explains how Omicron has a piece of RNA from HCoV-229E, a coronavirus that causes a common cold. Quoting (Nature) Predicting mammalian hosts in which novel coronaviruses can be generated,
Give that coronaviruses frequently undergo homologous recombination when they co-infect a host, and that SARS-CoV-2 is highly infectious to humans, the most immediate threat to public health is recombination of other coronaviruses with SARS-CoV-2.
Omicron contains a second recombinant mutation, ins214EPE. It came from another, unknown virus, or the human genome, by yet another, unknown mutation process. There are many unknown processes for which we see only the result.
Implications for the COVID future. Random replication errors are typically bad for a virus, or have no effect. Very rarely, they benefit, resulting in a more successful virus, with gain of function. A piece of genetic material grabbed “by mistake” from another successful virus has a much greater chance of change or gain of function.
What follows is my personal speculation. Each additional homologous mutation serves as a potential alignment point, increasing the possibility of subsequent successful homologous mutations. This, combined with the infectiousness of Omicron, implies an accelerating, spreading spectrum of recombinant mutations, hybridizing all coronaviruses capable of infecting humans.
The Merck drug molnupiravir may be fueling this. (Forbes) Supercharging New Viral Variants: The Dangers Of Molnupiravir (Part 1)
If (reverse) zoonosis is involved, the cane rat is a prime suspect. Domesticated live stock in southern Africa with a range down to Johannesburg, it is eerily evocative of the Wuhan Market. One date for the branching of Omicron is spring 2020. See (Twitter) Trevor Bedford for a tree. Could it have brewed since then in an immunocompromised individual without breaking out?
Is this the beginning of the end? Some optimistic voices point to the decline of Omicron in South Africa. (JAMA) Antibody Response and Variant Cross-Neutralization After SARS-CoV-2 Breakthrough Infection shows that a breakthrough delta infection creates a powerful immunity against delta; not general immunity against other strains.
The result of this coronavirus diversity may be a prolonged series of lesser eruptions, with the emergence of new clinical syndromes and strange diseases; see (AVMA) Coronavirus: Detailed taxonomy. This could be minimized with aggressive vaccine development. Equilibrium lies some years in the future.
Aw, heck. I’ve depressed you. It started funny and ended sad. No, viruses do not have sex, which probably depresses them also. All viruses are Frankenstein creations.